GEO DataSets

(Submitter supplied) We show that BRD9 suppresses osteoclastogenesis through negative feedback mechanism.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

2 Samples

Download data: XLS

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platform:

GPL24247

32 Samples

Download data: XLS

(Submitter supplied) We show that BRD9 suppresses osteoclastogenesis through negative feedback mechanism.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

12 Samples

Download data: XLSX

(Submitter supplied) We show that BRD9 suppresses osteoclastogenesis through negative feedback mechanism.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

16 Samples

Download data: XLSX

(Submitter supplied) We show that BRD9 suppresses osteoclastogenesis through negative feedback mechanism.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

2 Samples

Download data: TSV

(Submitter supplied) Macrophages induce a number of inflammatory response genes in response to stimulation with microbial ligands. In response to endotoxin Lipid A, lineage-defining and stimulation-responsive transcription factors cooperate to induce a gene activation cascade of primary followed by secondary response genes. Epigenetic state is an important regulator of the kinetics, specificity, and mechanism of gene activation of these two classes. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL19057 GPL21103

104 Samples

Download data: BEDGRAPH, TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

22 Samples

Download data: MTX, TSV

(Submitter supplied) We show that ARID1A promotes osteoclastogenesis

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

2 Samples

Download data: MTX, TSV

(Submitter supplied) We show that ARID1A promotes osteoclastogenesis

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

8 Samples

Download data: XLS

(Submitter supplied) We show that ARID1A promotes osteoclastogenesis

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

12 Samples

Download data: XLS, XLSX

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL30173

160 Samples

Download data: BW

(Submitter supplied) The non-canonical BAF complex (ncBAF) subunit BRD9 is essential for acute myeloid leukemia (AML) cell viability but has an unclear role in leukemogenesis. Because BRD9 is required for ncBAF complex assembly through its DUF3512 domain, precise bromodomain inhibition is necessary to parse the role of BRD9 as a transcriptional regulator from that of a scaffolding protein. To understand the specific role of BRD9 bromodomain function in regulating AML, we selected a panel of five AML cell lines with distinct driver mutations, disease classifications, and genomic aberrations and subjected them to short-term BRD9 bromodomain inhibition. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL30173

20 Samples

Download data: BW, CSV

(Submitter supplied) The non-canonical BAF complex (ncBAF) subunit BRD9 is essential for acute myeloid leukemia (AML) cell viability but has an unclear role in leukemogenesis. Because BRD9 is required for ncBAF complex assembly through its DUF3512 domain, precise bromodomain inhibition is necessary to parse the role of BRD9 as a transcriptional regulator from that of a scaffolding protein. To understand the specific role of BRD9 bromodomain function in regulating AML, we selected a panel of five AML cell lines with distinct driver mutations, disease classifications, and genomic aberrations and subjected them to short-term BRD9 bromodomain inhibition. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL30173

120 Samples

Download data: BW

(Submitter supplied) The non-canonical BAF complex (ncBAF) subunit BRD9 is essential for acute myeloid leukemia (AML) cell viability but has an unclear role in leukemogenesis. Because BRD9 is required for ncBAF complex assembly through its DUF3512 domain, precise bromodomain inhibition is necessary to parse the role of BRD9 as a transcriptional regulator from that of a scaffolding protein. To understand the specific role of BRD9 bromodomain function in regulating AML, we selected a panel of five AML cell lines with distinct driver mutations, disease classifications, and genomic aberrations and subjected them to short-term BRD9 bromodomain inhibition. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL30173

20 Samples

Download data: BW

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL24247 GPL24676

10 Samples

Download data: BW, TXT

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

4 Samples

Download data: BW

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

6 Samples

Download data: TXT

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

4 Samples

Download data: BIGWIG

(Submitter supplied) Chromatin remodeling caused by SWI/SNF (BAF) complexes is essential for regulating cell fates. Of these, BRD9, an essential component of the non-canonical BAF (ncBAF) complex, is post-transcriptionally decayed in multiple types of cancer, especially in myelodysplastic syndrome (MDS). However, how BRD9 loss or ncBAF disruption alters the HSCs' integrity remains unknown. Here, we identify that Brd9 loss enhances chromatin accessibility, promoting myeloid-lineage skewing at the expense of B cell development in vivo, followed by MDS development. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

4 Samples

Download data: BIGWIG

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24676

4 Samples

Download data: BIGWIG